https://journals.lww.com/co-endocrinology/
en-usThu, 24 May 2018 12:47:40 -0500Wolters Kluwer Health RSS Generatorhttps://images.journals.lww.com/co-endocrinology/XLargeThumb.01266029-201806000-00000.CV.jpeghttps://journals.lww.com/co-endocrinology/
https://journals.lww.com/co-endocrinology/Fulltext/2018/02000/Potential_mechanisms_underlying_the_effect_of.3.aspx
Purpose of review
Reduced energy intake, resulting from favourable changes in eating behaviour, is the predominant driver of weight loss following bariatric surgery. Here we review the most recent studies examining the impact of Roux-en-Y gastric bypass (RYGB) and sleeve gastrectomy, the two most common bariatric procedures, upon eating behaviour and the suggested underlying biological mechanisms.
Recent findings
Following RYGB or sleeve gastrectomy, most people report subjective changes in appetite, taste and food preference, with decreased high-fat preference most commonly reported. Objective postsurgery changes in taste and olfactory acuity occur. A new phenomenon, ‘meal-size aversion’, may contribute to reduced postoperative energy intake. Recent studies provide evidence for peptide YY3–36, glucagon-like peptide-1, ghrelin, neurotensin and oleoylethanolamide as mediators of postoperative eating behaviour changes. Factors modulating these changes include sex, type 2 diabetes status, genetics and bariatric procedure. New studies implicate central dopaminergic and opioid receptor signalling as key neural mediators driving altered eating behaviour. Brain neuroimaging studies show that obesity-associated changes in food-cue responses, brain connectivity and structural abnormalities are normalized following bariatric surgery.
Summary
Understanding the biological mechanisms mediating the eating behaviour changes engendered by bariatric surgery may lead to the development of novel therapeutic strategies for people with obesity.]]>Tue, 25 Oct 2011 09:21:40 GMT-05:0001266029-201802000-00003https://journals.lww.com/co-endocrinology/Fulltext/2018/02000/Noonan_syndrome___an_update_on_growth_and.12.aspx
Purpose of review
To provide an update on recent developments on Noonan syndrome with a special focus on endocrinology, bone, and metabolism aspects. The key issues still to be resolved and the future therapeutic perspectives will be discussed.
Recent findings
The discovery of the molecular genetic causes of Noonan syndrome and Noonan-syndrome-related disorders has permitted us to better understand the mechanisms underlying the different symptoms of these diseases and to establish genotype–phenotype correlations (in growth patterns for example). In addition to the classical clinical hallmarks of Noonan syndrome, new important aspects include decreased fertility in men, lean phenotype with increased energy expenditure and possible impact on carbohydrate metabolism/insulin sensitivity, and impaired bone health. Further clinical studies are needed to investigate the long-term impact of these findings and their possible interconnections. Finally, the understanding of the crucial role of RAS/mitogen-activated protein kinases dysregulation in the pathophysiology of Noonan syndrome allows us to devise new therapeutic approaches. Some agents are currently undergoing clinical trials in Noonan syndrome patients.
Summary
On the last 10 years, our knowledge of the molecular basis and the pathophysiology of Noonan syndrome has greatly advanced allowing us to gain insight in all the aspects of this disease and to devise new specific therapeutic strategies.]]>Tue, 25 Oct 2011 09:20:38 GMT-05:0001266029-201802000-00012https://journals.lww.com/co-endocrinology/Fulltext/2018/02000/Updates_on_the_biology_of_serotonin_and_tryptophan.4.aspx
Purpose of review
To summarize the most recent findings relevant to the biology of serotonin (5-hydroxytryptamine; 5-HT) and the enzyme tryptophan hydroxylase (TPH) in human gastrointestinal disease.
Recent findings
Serotonin is synthesized in the central nervous system (CNS) and the gastrointestinal tract where it is secreted from enteroendocrine cells. Its biosynthesis is regulated by two isoforms of the enzyme TPH of which TPH1 is localized predominantly in gastrointestinal enteroendocrine cells. Serotonin activates the peristaltic reflexes, regulates gastrointestinal motility, and has a role in intestinal inflammation. Inhibition of TPH with novel molecules represents a new pharmacological tool in the successful management of carcinoid syndrome in patients with gastrointestinal neuroendocrine tumors (GI-NETs). Certain 5-HT receptor subtype agonists and antagonists are useful in the treatment of functional gastrointestinal disorders.
Summary
The gastrointestinal tract is the largest storage organ for serotonin where its biosynthesis is regulated by TPH1. It has several important functions in gastrointestinal motility, secretion, and inflammation. Furthermore, TPH represents a target for inhibitory pharmacological therapy of serotonin access states such as the carcinoid syndrome.]]>Tue, 25 Oct 2011 09:21:09 GMT-05:0001266029-201802000-00004https://journals.lww.com/co-endocrinology/Fulltext/2018/02000/Endocrine_disrupters_and_pubertal_timing.9.aspx
Purpose of review
The current review summarizes recent epidemiologic data demonstrating the effects of endocrine disrupting compounds (EDCs) on the timing of puberty and highlights the complexity of understanding the interplay of environmental and genetic factors on pubertal timing.
Recent findings
In girls, there have been mixed results, with some exposures being associated with earlier timing of puberty, and some with later puberty. In boys, prepubertal exposures to nondioxin-like polychlorinated biphenyls accelerate puberty, whereas levels of insecticides, dioxin-like compounds, organochlorine pesticides, and lead delay puberty.
Summary
The effects of EDCs on pubertal timing are sexually dimorphic, compound specific, and varies according to the window of exposure. These studies confirm that low-level exposures to a mix of environmental compounds may mask the effects of individual compounds and complicate our ability to translate data from animal studies to human health and to fully understand the clinical implications of environmental epidemiology studies.]]>Thu, 16 Oct 2014 10:51:58 GMT-05:0001266029-201802000-00009https://journals.lww.com/co-endocrinology/Fulltext/2018/02000/Gender_dysphoria_in_youth___a_review_of_recent.8.aspx
Purpose of review
Transgender individuals including pubertal young people require hormonal therapy, in conjunction with mental health support. These youths are a unique population, with specific and individual desires and needs as they move through the physical and mental transition to the gender with which they identify.
Recent findings
The number of transgender youth presenting for treatment is increasing rapidly. They continue to have a high prevalence of mental health disorders, though not when supported in their sex identities by family in younger age. Older children are more susceptible to peer support or lack thereof. Treatment with gonadotropin-releasing hormone agonists remains a mainstay of early therapy, but is associated with high costs and decrease in bone mineral density; androgenic progestogens could be used as a lower cost alternative. Fertility preservation is discussed with the majority of transgender youth, but use of such services is low.
Summary
Transgender youth are an increasingly identified population in need of medical and mental health treatment, as well as social support throughout life.]]>Thu, 16 Oct 2014 10:52:33 GMT-05:0001266029-201802000-00008